Humans ; Rectal Neoplasms ; diagnosis ; therapy

Humans ; Neoplasms ; therapy ; Receptor, Epidermal Growth Factor

Breast Neoplasms ; diagnosis ; therapy ; Female ; Humans

Objective To study the protective mechanism of lycopene by its modulating lipid disturbance.Methods To make high fat diet model,the groups were intragastrically administered different dosage of lycopene at the same time.The lipids of serum and liver were measured.The pathological changes in liver were observed by HE staining method.Results Serum and liver TC,TG,LDL-C,AI levels in the three lycopene groups notably decreased(P

The present study is to investigate the protective actions of guggulsterone against the cytotoxicity produced by exposure to hydrogen peroxide (H2O2) in PC12 cells. It was evaluated by MTT [3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl-tetrazolium bromide] reduction assay, lactate dehydrogenase (LDH) release assay, and the release of nitric oxide (NO). ROS and Ca2+ in cells were evaluated by DCFH and Fura 2-AM, respectively. Mitochondrial membrane potential (MMP) was assessed by the retention of rhodamine 123 (Rh 123). Apoptosis and morphological alteration in PC12 cells were monitored with flow cytometry and electric microscope. Vitamin E, a potent antioxidant, was employed as a comparative agent. The results showed that preincubation of PC12 cells with guggulsterone (0.1-10 μmol·L-1) prevented cytotoxicity induced by H2O2. Extracellular accumulation of LDH, NO and intracellular accumulation of ROS, Ca2+ resulting from H2O2 were significantly reduced by guggulsterone. Incubation of cells with H2O2 caused a marked decrease in MMP, which was significantly inhibited by guggulsterone. The percentage of H2O2-induced apoptosis in PC12 cells was 24.3%, and decreased in the presence of guggulsterone (0.1-10 μmol·L-1) by .8.4%, 15 .9%, 11.8%, respectively. Guggulsterone exhibited comparable potency against oxidative stress induced by H2O2 in PC12 cells as that of vitamin E. The present findings showed that guggulsterone attenuated H2O2-induced cytotoxicity, extracellular accumulation of LDH and NO, intracellular accumulation of ROS and Ca2+, loss of MMP, and apoptosis, which may represent the cellular mechanisms for its neuroprotective action.

Objective To explore the mechanism of apeptosis in rheumatoid arthritis synoviocyte induced by dihydroartemisinin. Methods Synovial tissues were cut from rheumatoid arthritis patients when who was under knee prosthesis. Apoptosis was detected with flow cytometry. Western blot was performed to assess ser473-phosphorylated Akt. EMSA (electrophoretic mobility shift assay) was used to ana-lyze NF-κB activation. Results Dihydroartemisin can induce apoptosis in rheumatoid arthritis synoviocyte in a dose-dependent manor from 2.5μmol/L to 10μmol/L. Rheumatoid Arthritis synoviocyte cultured with dihydroartemisinin in 5μmol/L or 10μmoL/L can significantly in-hibit serine 473 phosphorylation in Akt and activation of NF-κB. Conclusion Dihydroartemisinin can induce apoptosis in rheumatoid arthri-tis synoviocyte through Akt signal pathway.

Chemotherapy, Adjuvant ; Humans ; Stomach Neoplasms ; drug therapy

Vehicle driver fatigue is an important factor in traffic accidents.This paper introduced three kinds of detecting techniques,namely driver's physical signals and individual characteristics,vehicle parameters,and five detecting devices.But there still are limitations of the mentioned detecting techniques and devices in the paper.The problems and developing trend are briefly analyzed.